摘要:这3名患者在取得稳定的分子学缓解之后(融合基因转阴PCRU)停用达沙替尼。1名患者复发,另外两名患者在1年后仍保持了PCRU。以前说过,达沙替尼确实可以提高免疫力,希望今后能获得更多的相关研究报告。
; \8 S( E c. l6 n( {6 O 关于这个研究值得注意的是,这三名患者都是服用格列卫失败后转用达沙替尼的,也即他们对格列卫是耐药的。这与法国的格列卫停药研究又有所不同,那个研究中的患者都是对格列卫反应良好的。希望医生们能扩大研究长期观察,看看停用达沙替尼是否能持久不复发。
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0 H6 Z8 X1 V' Z, a, e7 B, f作者:来自澳大利亚5 C$ A" x" c& u3 M3 e4 l
来源:Haematologica. 2011.8.9.
: i2 `- m$ Z" ?1 {) `4 S+ [Dear Group,
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, Z$ j, g8 f# ~5 {% xSome of you are on Dasatinib (Sprycel) and we wish to give news on all CML1 ?3 S0 \3 `9 k; K# X5 f: m5 B
therapies. Here is a report from Australia on 3 patients who went off Sprycel
7 C8 ?% b5 }. D, E5 F. qafter stable molecular response (PCRU). 1 patient relapsed but 2/3 patients
/ O" U; O- }9 o: z8 v& G6 y% Iremain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel: g7 S; e! @6 c, `; x; Z& C8 H
does spike up the immune system so I hope more reports come out on this issue.7 z3 @; ]0 f# I6 K
* V. o6 R" T1 W% U/ J2 ]) ?The remarkable news about Sprycel cessation is that all 3 patients had failed) z, m3 k; [3 E6 G6 v3 T
Gleevec and Sprycel was their second TKI so they had resistant disease. This is4 `" |* s5 y' d
different from the stopping Gleevec trial in France which only targets patients
r5 W9 S: Y" `who have done well on Gleevec.: A& B( J: O7 h/ m" L" L
9 W( G5 h5 t7 B5 v% AHopefully, the doctors will report on a larger study and long-term to see if the
- e2 U) o: j9 r/ S+ q: Xresponse off Sprycel is sustained.
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4 [' U8 x7 S$ C- P, a! bBest Wishes,
3 e4 g1 T; Y! z; b8 Q- JAnjana# E: c( L7 u" H3 N
2 K. T1 ^5 _/ H. a$ b. v G7 p5 k5 l8 X0 c% ?0 o& M
0 h# [' Z6 W6 J0 E; AHaematologica. 2011 Aug 9. [Epub ahead of print]+ g i% P! C* l. R" U
Durable complete molecular remission of chronic myeloid leukemia following
3 h+ ]/ e6 X2 J( N- q( i ]5 D4 ^" Bdasatinib cessation, despite adverse disease features.
+ F/ O4 A c# i2 {( J; fRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.& O# E0 P' Y& E2 r' X
Source5 }! _: |+ m P- M3 l
Adelaide, Australia;
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' @: E9 }( G4 ?1 yAbstract
4 H6 ]/ M* s& G% C2 mPatients with chronic myeloid leukemia, treated with imatinib, who have a; B9 ~, n5 E ~5 q' M: X( `4 m
durable complete molecular response might remain in CMR after stopping3 l' e! J. Q9 o% t' A. c- p
treatment. Previous reports of patients stopping treatment in complete molecular2 b1 O' f# ?5 a* e
response have included only patients with a good response to imatinib. We) T c3 P0 Y7 a) p* m$ r
describe three patients with stable complete molecular response on dasatinib
6 b6 @7 a. f' A' l9 ktreatment following imatinib failure. Two of the three patients remain in7 b+ E5 s! B- m7 {0 _
complete molecular response more than 12 months after stopping dasatinib. In8 e0 L1 E8 ?6 o
these two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to, f& a( h i( ^7 H9 ^5 r
show that the leukemic clone remains detectable, as we have previously shown in
4 m, y3 f4 r7 Z) E. I/ Dimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
3 z" z) v4 k" Q! G! Wthe emergence of clonal T cell populations, were observed both in one patient
5 R: U; ]* E Zwho relapsed and in one patient in remission. Our results suggest that the8 _) d0 r9 b. g! h$ Z; m- p
characteristics of complete molecular response on dasatinib treatment may be
: c, Y& C9 |, R7 n4 ]3 z+ d8 gsimilar to that achieved with imatinib, at least in patients with adverse9 t0 p9 v* P( X/ z& w _7 Z+ `
disease features." s5 f% M$ |! M) x' f
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